Due to the overwhelming popularity of Dr. Salim Rezaie‘s recent post discussing the Brugada criteria for SVT with aberrancy vs VT, Dr. Jason West (@JWestEM, an EM resident from Jacobi/Montefiore) kindly helped to co-author and package this information into a PV card for quick reference. To use this sequential, four-question approach, if at any time you answer YES to the question, it is ventricular tachycardia.
The incidence of critical illness in the ED is rising, with greater than 1 million ED patients requiring emergent resuscitation each year. In addition to definitive airway management, hemodynamic support is among the most important life-saving interventions implemented by emergency physicians. When a patient develops persistent hypotension, what is your approach to choosing the right vasopressor medication for hemodynamic support?
Persistent hypotension results in impaired tissue perfusion and is often a late and ominous indication of decompensated shock. Correction of persistent hypotension is imperative, often requiring vasopressors and inotropes. When considering an agent for hemodynamic support, the following checklist can guide your choice: 1–4
1. Why is the patient hypotensive?
Identifying the cause of the hypotension will allow you to select an agent targeted to the source of the problem. Causes of hypotension include hypovolemia, impaired vascular tone, impaired pump function, or some combination of these problems.
2. Have I optimized volume status and ruled out other diagnoses?
Initial management of the hypotensive patient should target optimizing intravascular volume prior to initiating a vasoactive medication. Vasopressors or inotropes cannot improve malperfusion secondary to isolated hypovolemia (such as hemorrhage, gastrointestinal bleeding or severe dehydration), and use of these agents prior to volume resuscitation can exacerbate existing metabolic derangements. Unrelated conditions that impair preload or cardiac output, including tension pneumothorax and pericardial tamponade, should also be considered prior to initiating vasoactive therapy.
3. How can I pharmacologically redirect blood flow to improve the problem?
Selecting an agent for hemodynamic support is analogous to choosing an antibiotic for infection. You are best guided by matching medication activity to the underlying pathology of the illness.
- Problem with VASCULAR TONE? Phenylephrine is the only agent with exclusive activity at α adrenergic receptors, and vasopressin is the only agent with activity at vasopressin receptors. In this sense, these are pure pressor agents and have no direct impact of pump function. Hypotension from isolated loss of vascular tone is uncommon but can be caused by loss of sympathetic tone from spinal cord injury (“neurogenic shock”).
- Problem with PUMP FUNCTION? Hypotension attributable to isolated acute myocardial compromise can be improved with pharmacologic agents that increase inotropy and contractility. This includes any agent with action at β1 , β2 or dopaminergic receptors. Dobutamine and isoproterenol are the only agents with exclusive activity at β adrenergic receptors. Generally, these are pure intropes and have no vasoconstrictive properties. Hypotension from isolated pump failure can be caused by acute decompensated heart failure or acute coronary syndrome.
- MULTIFACTORIAL problem? Problems that impact both vascular tone and cardiac function require medications that operate at multiple receptors. These include epinephrine, norepinephrine and dopamine. The physiologic impact of dopamine is dose dependent, with preferential increases in pump function at lower doses. Examples of disorders that impact both pump and tone include anaphylaxis (see “Dirty Epi” drip) or septic shock.
4. Will I be limited by side effects of my pressor choice?
Side effects of vasoactive medications are related both to the direct mechanism of action of the agent, as well as the compensatory mechanisms precipitated by them. Concerning side effects of inotropes include dysrhythmias and increased myocardial oxygen demand, whereas vasopressors can cause undesired limitations in blood flow to the gut and kidneys.
|Agent||Primary Receptor||Primary Impact||Potential side effect||Prototypical clinical scenario|
|Phenylephrine||α1||Increased SVR||Reflexive decreased HR||Neurogenic shock|
|Vasopressin||V||Increased SVR||Decreased splanchnic flow||Adjunct for septic shock|
|Dobutamine||β1, β2||Increased inotropy||Transient decreases in SVR (β2 agonsim)||Cardiogenic shock from late-stage heart failure|
|Dopamine (low-dose)||D, β1||Increased inotropy and heart rate||Tachydysrhythmias||Cardiogenic shock, particularly if bradycardic|
|Epinephrine||α1, α2, β1, β2||Increased SVR and inotropy||Tachydysrhythmias and decreased splanchnic flow||Anaphylaxis|
|Norepinephrine||α1, α2, β1>> β2*||Increased SVR and inotropy||Decreased splanchnic and renal flow||Septic shock|
|Dopamine (high-dose)||D, α1, β1>> β2*||Increased SVR and inotropy||Tachydysrhythmias and decreased splanchnic/renal flow||Bradycardic cardiovascular collapse|
|* Controversial whether norepinephrine and high-dose dopamine have any β2 effects. If any, it is likely very low.|
5. When choosing between similar agents, does evidence support use of a specific agent over another?
The majority of evidence comparing pressors head-to-head has been done in patients with septic shock; the largest amount of data has compared high-dose dopamine to norephinephrine. Based on this data, norepinephrine has been associated with lower incidence arrythmias and improved mortality when compared to dopamine.
Epinephrine has been compared with several other regimens both in septic shock and undifferentiated shock. When epinephrine was compared to norepinephrine and dobutamine, all of the agents were equally effective in achieving hemodynamic goals, though epinephrine was associated with increased incidence of tachydysrhythmias and prolonged metabolic derangement when compared to other agents. There was no difference in mortality. Robust data comparing other similar agents in other disease processes are lacking.
Myburgh J, Higgins A, Jovanovska A, et al. A comparison of epinephrine and norepinephrine in critically ill patients. Intensive Care Med. 2008;34(12):2226-2234. [PubMed]
Ellender T, Skinner J. The use of vasopressors and inotropes in the emergency medical treatment of shock. Emerg Med Clin North Am. 2008;26(3):759-86, ix. [PubMed]
Vasu T, Cavallazzi R, Hirani A, Kaplan G, Leiby B, Marik P. Norepinephrine or dopamine for septic shock: systematic review of randomized clinical trials. J Intensive Care Med. 2012;27(3):172-178. [PubMed]
De B, Aldecoa C, Njimi H, Vincent J. Dopamine versus norepinephrine in the treatment of septic shock: a meta-analysis*. Crit Care Med. 2012;40(3):725-730. [PubMed]
It’s 7 am on a Monday. Your first patient is an 82 year-old woman who was brought in by EMS from an assisted living facility. All EMS can tell you is that she was not acting herself. You enter her room and introduce yourself. “Hello Mrs. Jones. How are you today?” The woman startles, “Well, you see, I went to put my dog out, and then I was just walking, and couldn’t remember. So it’s all coming full circle, and then I ate a sandwich.” Just then EMS rolls in with another patient, a 75 year-old male coming from home, who was found by his wife in his recliner minimally responsive, with a GCS of 6. He is followed by a 76 year-old female who had a fall from standing three days ago, and has been increasingly confused today, and is currently oriented only to person.
Airway management is one of the defining skills of an emergency physician, but our role in the care of intubated patients may continue long after endotracheal tube placement is confirmed. In mechanically ventilated patients, acute elevations in airways pressures can be triggered by both benign and life-threatening causes. When the ventilator alarms, do you know how to tell the difference? What is your approach in troubleshooting the potential problems?
Differentiating between SVT with aberrancy and VT can be very difficult. It is crucial to be able to make this distinction as therapeutic decisions are anchored to this differentiation. Brugada et al prospectively analyzed 384 patients with VT and 170 patients with SVT with aberrant conduction to see if it was possible to come up with a simple criteria to help differentiate between the two with high sensitivity and specificity.
EKGs are a simple, cheap modality that can give an emergency physician quite a bit of information. Sometimes, in a busy ER, this information can be very subtle and almost overlooked without a second thought. A perfect example of this is a New Tall T-wave in lead V1 (NTTV1). This finding can be a normal variant, but can also be a precursor to badness.
A 25 year old woman presents to the Emergency Department having syncopized in the waiting room, where she was triaged with the chief complaint of abdominal pain. Ectopic pregnancy immediately bubbles to the top of your differential diagnosis. The patient is too dizzy to walk to the bathroom to give you a urine specimen to check a urine pregnancy test. Plus, she admits that she just urinated in the waiting room bathroom a few minutes ago – so no urine now.
Trick of the Trade
Apply several drops of whole blood (instead of urine) into the pregnancy test cassette. In the photo below, the patient was pregnant with a serum beta-HCG level of 250 mIU/mL whose urine and whole blood qualitative tests were both positive.
Did you know that most urine pregnancy test kits are approved for both urine and serum samples? On a quick Google search, I found that Accutest, Cardinal Health, ICON, OSOM, and Rapid Response all are approved for both. The question is whether this will work for whole blood.
One study 1 in the Journal of Emergency Medicine by Dr. Fromm from Maimonides Medical Center looked at exactly this issue. Whole blood pregnancy test performed extremely well, especially if positive:
- Sensitivity 95.8%
- Specificity 100%
- Negative predictive value 97.9%
- Positive predictive value 100%
In their study, very low beta-HCG values (<159 mIU/mL) occasionally yielded a false negative for whole blood pregnancy tests. The whole blood testing approach missed a total 9 of 425 pregnancies. Interestingly, the urine pregnancy test was also negative in 5 of those 9 and not performed in the other 4.
Believe a positive test. Confirm all tests with a urine qualitative test or quantitative serum beta-HCG.
- Be sure to wait at least 5 minutes when using whole blood in the kit. It sometimes takes a while.
- Do not apply additional drops of water or saline to the whole blood sample. This causes unnecessary dilution. Just wait for the blood to osmose across the entire test strip.
- This is trick is ONLY for medical professionals and not the lay public. We are discussing an actual blood draw and not a simple cut on a finger to obtain blood.
Another example courtesy of Dr. Joe Habboushe (New York Hospital–Queens of Cornell University) and Dr. Graham Walker (Stanford) 2 :
S = Sample well; T = Test specific (will show bar if +HCG); C = Control (will always have a bar)